tbuckley/cabot-search huggingface dataset:
POS0972 INCREASED RISK FOR STROKE IN PATIENTS WITH FAMILIAL MEDITERRANEAN FEVER, RESULTS FROM A LARGE POPULATION-BASED STUDY
Authors: N. Ben-Shabat, O. Gendelman, L. Fisher, U. Shani, Y. S. Patt, D. Mcgonagle, A. Watad, H. Amital
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> The association between chronic inflammatory conditions and cardiovascular disease is well established. Considering Familial-Mediterranean-Fever (FMF), few studies exist investigating the risk of ischemic heart disease, and none address the risk of stroke. <h3>Objectives</h3> To evaluate the incidence and risk for stroke in FMF patients compared to the general population. <h3>Methods</h3> A retrospective cohort study using the electronic database of Clalit Health Services (CHS), the largest health organization in Israel. All FMF patients diagnosed between 2000-2016 were included and matched with control according to age, gender, and place of residence. Follow-up continued until the first diagnosis of stroke or death. The incidence of stroke was compared between the groups using univariate and multivariate models adjusting for cardiovascular risk-factors. <h3>Results</h3> 9,769 FMF patients and a similar number of controls were followed up for a median period of 12.5 years. The mean age at the beginning of the follow-up was 25.7 years. 208 FMF patients were diagnosed with stroke compared to 148 controls, resulting in an incidence rate (per 10,000 persons-years) of 19.8 (95%CI 17.2-22.7), and 13.9 (95%CI 11.8 to 16.4) respectively, and a crude HR of 1.42 (95% CI 1.15 to 1.76; p&lt;0.001). In a multivariate analysis, FMF patients who developed amyloidosis with related or non-related renal failure demonstrated significant stroke risk (HR=2.16; 95%CI 1.38 to 3.38; P&lt;0.001), as well as for those who did not develop these complications (HR=1.32; 95%CI 1.04 to 1.67; P&lt;0.05). <h3>Conclusion</h3> FMF patients are at increased risk for stroke regardless of known complications. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
POS0982 UNUSUAL PRESENTATION OF LEWIS-SUMNER SYNDROME IN ELDERLY SIMULATING POLYMYOSITIS AND POLYMYALGIA RHEUMATICA
Authors: M. Brahem, R. Sarraj, O. Jomaa, B. Jebali, S. Abdellatif, H. Hachfi, Y. Mohamed
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Lewis-Sumner syndrome (LSS) or multifocal acquired demyelinating sensory and motor neuropathy (MADSAM) is an atypical form of chronic inflammatory demyelinating polyneuropathy (CIDP). This rare disease is characterized by a predominantly distal, asymmetric weakness mostly affecting the upper limbs and motor dysfunction with adult onset. Diagnosis can be difficult to establish if the clinical presentation is atypical and frequently simulates inflammatory myopathy. <h3>Objectives:</h3> <h3>Methods</h3> We report a rare case of LSS in an old patient with unusual clinical aspects. <h3>Results</h3> A 70-year-old female patient with a history of atrial fibrillation complicated by pulmonary embolism, presented with myalgia and muscle weakness of the shoulders, upper arms, hips and thighs. This involvement was bilateral, symmetrical and evolving since 3 months, causing difficulties in climbing stairs, standing or walking. Physical examination showed a proximal muscle deficiency affecting proximal muscles of the upper and lower limbs. In this stage we suspected a poly yositis or polymyalgia rheumatica. We completed by biological assessment that showed a biological inflammatory syndrome (ESR at 90 mm at first hour; CRP at 80 mg/L) and elevated lactate dehydrogenase level at 490 IU/L. The immunoblot polymyositis profile (anti-Mi2, anti-Ku, anti Pm/SCL, anti-Jo1, anti-PL12, anti-PI7, anti-SSA 52kDa, anti-EJ, anti-OJ and anti-SRP) was negative. The MRI of lower limbs revealed a signal abnormality in the gluteus medius muscles on both sides with inflammatory appearance. The Electromyography revealed sensorimotor neuropathy affecting the four extremities with motor nerve conduction blocks. This aspect was in favor of LSS, so we completed by a cerebrospinal fluid study which revealed a proteinorachia at 0.4g/l with normal glycorachia and normal cell counts. These results confirmed the diagnosis of LSS. The patient was treated by corticosteroids at dose of 1 mg/ kg/ day during 2 months, with a progressive decrease of treatment. The evolution was marked by a spectacular clinical and biological response. <h3>Conclusion</h3> LSS is a very rare disease that can simulate inflammatory myopathy and polymyalgia rheumatica in elderly. So, it should be suspected in old patients suffered from proximal muscle deficiency. <h3>Reference</h3> [1]H. Assadeck et al, Bull. Soc. Pathol. Exot. (2018) <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
POS0995-HPR SLE-DAS AS AN ALTERNATIVE TOOL TO MEASURE ACTIVITY OF SYSTEMIC LUPUS ERYTHEMATOSUS: COMPARISON WITH SLEDAI-2K, IN A POPULATION FROM THE DOMINICAN REPUBLIC. PILOT STUDY
Authors: L. Perez Rodriguez, R. A. Alvarez Santana, D. Garcia, T. Polanco Mora, L. Concepción Sanchez, I. Paulino, I. Mercedes, E. Rodriguez Bautista, T. Valdez, A. Feriz, R. Muñoz Louis
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that mainly affects women. Efforts are currently being made to validate the Systemic Lupus Erythematosus Disease Activity Score (SLE-DAS), since it allows quantifying the magnitude of the findings as opposed to an arbitrary value of present or absent in the renal, joint, hematological and serological spheres. <sup>[2]</sup> <h3>Objectives</h3> To evaluate the activity of Systemic Lupus Erythematosus with the SLE-DAS tool, comparing it with SLEDAI2-K. <h3>Methods</h3> Descriptive, observational, transversal. Patients from the Rheumatology Service of the Padre Billini Teaching Hospital were evaluated between October-December 2022. Inclusion criteria: &gt; 18 years, SLE according to the EULAR/ACR 2019 classification criteria. Exclusion criteria: diagnosis of another autoimmune disease, patients with cognitive deficits. SLE-DAS tool: Inactive ≤2.08, mild 2.08 - 7.64, moderate/severe &gt;7.64, SLEDAI: Inactive: &lt;3, Mild to moderate: 3/12, severe &gt;12. Descriptive analysis and Spearman's rho (ρ) correlation using SPSSv23. <h3>Results</h3> 92 patients met inclusion criteria. 95.7% (88) female, mean age 41.5 ± 12 years, mean SLE 8.2 years. AHT 29.3% (27), DM 7.6% [7], lupus nephritis 35.8% (33), Obesity 7.6% [7], musculoskeletal 20.6% (19), Vasculitis 6.5% [6], Neuro Lupus 4.3% [4], antimalarials 96.7% (89), glucocorticoids 39.1% (36), Mycophenolate Mofetil 40.2% (37), Rituximab 7.6% [7], Methotrexate 5.4% [5], Azathioprine 4.3% [4], Tacrolimus 2.1% (2), Cyclophosphamide 1.1% [1]. SLE-DAS inactive: 81.5% (75) vs SLEDAI inactive: 88% (81), SLE-DAS inactive: 81.5% (75) vs SLEDAI inactive: 88% (81) (Spearman's rho (ρ)= -0.11), a gradient difference of 6.5% [6]. <h3>Conclusion</h3> Our study demonstrated a significant inverse correlation in the correlation between SLE-DAS vs. SLEDAI in inactive patients, supporting that the use of the SLE-DAS may be more sensitive to assess activity or changes in the clinical course of patients with SLE. More studies are needed to validate this tool and standardize it for our population. <h3>References</h3> [1]Zucchi, D. et al. (2019) One Year in review 2019: Systemic lupus erythematosus, Clin Exp Rheumatol. Available at: https://www.clinexprheumatol.org/abstract.asp?a=14436 (Accessed: December 12, 2022). [2]Jesus, D. et al. (2019) "Derivation and validation of the SLE disease activity score (SLE-Das): A new SLE continuous measure with high sensitivity for changes in disease activity," Annals of the Rheumatic Diseases, 78(3), pp. 365–371. Available at: https://doi.org/10.1136/annrheumdis-2018-214502. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0112 IT IS SAFE AND EFFECTIVE TO USE HUMAN CXCL5 TO TREAT MURINE LUPUS
Authors: D. Guo, F. Lim, C. T. Ng, A. Low, X. Fan
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> As a novel myeloid/neutrophil-targeting therapy for systemic lupus erythematosus (SLE), the therapeutic efficacy of administering mouse (<i>m</i>)CXCL5 to lupus-prone mice have been demonstrated by our group recently<sup>[1,2]</sup>. <h3>Objectives</h3> The aim of this study is to examine the pre-clinical safety and establish the pharmacokinetic (PK) response of human (<i>h</i>)CXCL5 to ease the commercialization and bring our discovery from bench to bedside. <h3>Methods</h3> Immediate and accumulative liver and kidney toxicity were determined by alanine transaminase and aspartate transaminase activity and urinary albumin-to-creatinine ratio (ACR). <i>m</i>CXCL5 expression in major internal organs (e.g., kidneys, lungs, liver, heart, brain and spleen) was determined by immunofluorescent staining on snap-frozen sections. Whether administering <i>h</i>CXCL5 promoted cancer cell growth was examined in both <i>in vitro</i> and <i>in vivo</i> renal cell carcinoma models. Haematological toxicity and circulating immunity, cell counts for white blood cells, red blood cells, monocytes, neutrophils, T cells and B cells, were evaluated in both Institute of Cancer Research (ICR) healthy and MRL/lpr (Fas<sup>lpr</sup>) lupus-prone mice. PK study of <i>h</i>CXCL5 was performed in both ICR healthy and Fas<sup>lpr</sup> lupus-prone mice intravenously. <h3>Results</h3> Our study showed that it was safe to administer CXCL5. There was no liver or kidney toxicity or cancer inducing effects. There was no further inflammation caused by <i>h</i>CXCL5 administration. Major components of the immune system were also not compromised. PK study showed that blood endogenous <i>m</i>CXCL5 levels were not altered by exogenous <i>h</i>CXCL5 administration in ICR healthy mice, but increased in Fas<sup>lpr</sup> lupus-prone mice. Blood exogenous <i>h</i>CXCL5 was only detectable within 24 hours post-administration and the peak levels were positively correlated with the administration dosage. Mice survival was improved and reversely correlated with administration dosage. <h3>Conclusion</h3> It is safe and effective to use <i>h</i>CXCL5 to treat murine lupus. <h3>References</h3> [1]Fan X, Ng CT, Guo D, et al. CXCL5 administration dampens inflammation and improves survival in murine lupus via myeloid and neutrophil pathways. <i>Arthritis Rheumatol</i>. Oct 14 2022;doi:10.1002/art.42383 [2]Phillips R. CXCL5 effective in mouse model of SLE. <i>Nat Rev Rheumatol</i>. Dec 2022;18(12):673. doi:10.1038/s41584-022-00869-2 <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0143 VORINOSTAT IMPROVES THE PATHOGENESIS OF SLE MODEL MICE BY SUPPRESSING IFN-I AND TLR7/8 SIGNALS
Authors: T. Hirayama, H. Konaka, Y. Kato, H. Takamatsu, A. Kumanogoh
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> SLE is a systemic autoimmune disease caused by impaired innate and acquired immune tolerance, resulting in increased Type I IFN (IFN-I) and aberrant B cell development, in which cGAS and TLR 7/8 signaling play critical roles. TLR7/8 and cGAS signal is activated due to the overresponse to nucleic acid derived from impaired clearance of apoptotic cells, which leads to increased IFN-I production. Activation of TLR7/8 signaling also leads to the development of abnormal B cell populations, including short-lived plasma blasts, double negative B cells (DNB), and active native B (NAB). It suggests that signaling pathway via TLR7/8 and cGAS would be a good therapeutic target for SLE. Therefore, we screened agents that inhibit the induction of interferon-stimulated genes (ISGs) by LPS, R848 or cGAMP stimulation using an approved drug library and found that vorinostat inhibits ISG induction upon cGAMP and LPS stimulation. <h3>Objectives</h3> The purpose of this study is to elucidate the mechanism by which vorinostat suppresses IFN-I production and to demonstrate that vorinostat improves the severity of the disease phenotype in SLE-prone mice. <h3>Methods</h3> We investigated the effect of vorinostat on the expression and phosphorylation of TBK1, IRF3, IRF5, and IRF7, upon LPS or cGAMP stimulation, as well as on the in vitro differentiation of human B cells into plasma cells by a culture medium containing R848. Additionally, the effect of Vorinostat on the severity of SLE-prone mice, such as NZB/W F1 mice and SAVI mice with point mutations in STING, was also investigated. <h3>Results</h3> Vorinostat inhibited TBK1 phosphorylation and subsequent nuclear translocation of IRF3 and expression of IRF5 and IRF7. Consequently, the expression of IFN-β and ISGs were suppressed. Additionally, differentiation of human B cells cultured in R848-containing medium into plasma cells was inhibited in the presence of vorinostat. Furthermore, vorinostat improved the disease severity of NZB/W F1 mice, including survival, proteinuria, and glomerulonephritis, and decreased autoantibody titer and TLR7 expression. Vorinostat also ameliorated the lung inflammation and fibrosis, and interstitial nephritis in SAVI mice by inhibiting the ISG expression. <h3>Conclusion</h3> We found vorinostat ameliorates the disease severity of SLE prone mice by inhibiting IFN-I production and pathogenic B cell development via suppressing the downstream signal of TLR7/8 and cGAS. This finding represents a new therapeutic candidate for SLE. <h3>REFERENCES:</h3> NIL. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0393 SLEEP DISORDERS IN PATIENTS AFFECTED WITH RHEUMATOID ARTHRITIS: ASSESSMENT AND CORRELATION WITH FLARE-UPS
Authors: M. Ghanmi, S. Mtawaa, N. El Fani, M. Gaddour, W. Wanes, S. Jemni
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Patients with rheumatoid arthritis (RA) suffer from augmented inflammatory pain during flare-ups. Their quality of sleep (QOS) is altered, but to the best of our knowledge no local data has been published on the matter. <h3>Objectives</h3> We aim to assess the quality of sleep in Patients with RA and to study its correlation with the disease flare-ups. QOS was altered among patients with RA. Poor sleep quality has been linked to pain, mood, fatigability, stress, and disease activity in the rheumatic disease population [1]. This study established the link between flare-ups and the presence of sleep disorders. We found greater frequence of sleep disturbance in this population [1] which may be explained by the presence of more patients with higher DAS28. <h3>Methods</h3> We conducted a cross sectional study using a self-administered questionnaire. Patients with RA consulting in physical medicine and rehabilitations outpatient clinics were included. Data was collected during the period from September 1, 2020 until the end of Mai 2022. We collected sociodemographic and clinical data. Disease Activity Scale (DAS28) greater than 5.1 was used to define a flare-up. QOS was assessed using the Pittsburg Sleep quality index (PSQI) in its validated Arabic version. Sleep disorder was defined by PSQI greater than 5. <h3>Results</h3> We included 54 patients. Their mean age was 38.6. Mean duration of progression of the disease was 6.9 years. Almost half of the patients were having a flare-up (42.6%). Mean score of PSQI was 9.6. 82.5% of the patients had a sleep disorder. The most common sleep disorder was multiple nocturnal wake ups (94.4%). We found a significant correlation between sleep disorder and a rheumatoid flare. Odds Ratio was 11.8 (p= 0,012). <h3>Conclusion</h3> QOS was altered among patients with RA. Poor sleep quality has been linked to pain, mood, fatigability, stress, and disease activity in the rheumatic disease population [1]. This study established the link between flare-ups and the presence of sleep disorders. Clinicians dealing with patients with patients with RA should have more attention to the QOS especially on flare-ups. <h3>Reference</h3> [1]Westhovens R, Van der Elst K, Matthys A, Tran M, Gilloteau I. Sleep problems in patients with rheumatoid arthritis. <i>J Rheumatol</i>. 2014;41(1):31–40. doi: 10.3899/jrheum.140167 <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0055 THE ROLES OF OX40L AND TNF BISPECIFIC ANTIBODY IN OSTEOCLASTOGENESIS
Authors: H. S. Kwon, J. Y. Kim, S. U. Kim, J. S. Lee, H. R. Kang, S. Ban, E. Y. Lee
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Rheumatoid arthritis (RA) is a chronic, inflammatory disease that leads to progressive cartilage and bone destruction. OX40 ligand (OX40L) is expressed predominantly on antigen-presenting cells and highly associated with joint inflammation in RA<sup>[1]</sup>. Yet, the role of OX40L in osteoclastogenesis is unclear. <h3>Objectives</h3> In this study, we investigated the effects of dual blocking of TNF and OX40L by bispecific antibody (IMB-101) on RANKL-induced osteoclastogenesis. <h3>Methods</h3> CD14+ monocytes were isolated from peripheral blood mononuclear cells (PBMCs) of healthy donors (n=6). CD14+ monocytes were cultured with M-CSF (20ng/ml) and RANKL (40ng/ml) for 6 to 7 days in the presence of TNF antibody, OX40L antibody, or bispecific antibody. TRAP-positive multinucleated giant cells (&gt;3 nuclei/cell) were counted as osteoclast. PU.1, RANK and NFATc1, markers of osteoclast differentiation were assessed by the quantitative reverse transcription PCR (RT-qPCR). The expression of OX40L was analyzed in the presence of RANKL or TNF at the early and late stage of osteoclast differentiation. <h3>Results</h3> The expression of OX40L was increased by RANKL and TNF at the early stage of osteoclast differentiation (day 3) in a TNF dose-dependent manner. IMB-101 decreased RANKL-induced osteoclastogenesis via downregulating NFATc1 expression (Figure 1). IMB-101 further reduced PU.1, RANK and NFATc1 expression during early stage of osteoclast differentiation (day 3) compared to TNF inhibitor or TNF inhibitor and OX40L inhibitor (n=3). <h3>Conclusion</h3> Our data suggested that IMB-101 might have a beneficial effect on imbalance of the bone resorption in RA especially by suppressing osteoclast differentiation. <h3>Reference</h3> [1]Yoshioka, Taro et al. "Contribution of OX40/OX40 ligand interaction to the pathogenesis of rheumatoid arthritis." <i>European Journal of Immunology</i> 30 (2000): n. pag. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0211 ASSESSMENT OF STIGMATIZATION IN RHEUMATOID ARTHRITIS USING THE STIGMA SCALE FOR CHRONIC ILLNESSES-SHORT FORM (SSCI-8)
Authors: L. Rouached, E. Hannech, S. Bouden, A. Ben Tekaya, R. Tekaya, I. Mahmoud, O. Saidane, L. Abdelmoula
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Rheumatoid arthritis (RA) is a chronic inflammatory disease that occurs among productive patients. It often causes functional disability that can be permanent, with both physical and mental impact. <h3>Objectives</h3> We aimed to assess the degree of stigmatization and associated factors in patients with RA. <h3>Methods</h3> This was a cross-sectional study including patients with RA. Sociodemographic, clinical, paraclinical, and therapeutic data were collected. Stigma was assessed using the Stigma Scale for Chronic Illnesses-Short Form (SSCI-8) [1]. This scale is composed of 8 items. Responses for each item are made as follows: 1 = never, 2 = rarely, 3 = sometimes, 4 = often, and 5 = always. The range of raw scores assigned for the SSCI-8 was 8 to 40. The closer the score was to the upper value, the greater the degree of stigma. <h3>Results</h3> These were 100 RA patients: 81 women (81%) and 19 men (19%). The mean age was 55.33±10.08 years [25-76]. The mean disease duration was 14.21±10.10 years [1-46]. RA was immunopositive in 50% of patients. It was erosive in 75% of cases. Coxitis was present in 6 patients. The mean disease activity measured by DAS28-CRP was 3.81±1.56 [0.12-6.90]. The mean value of functional impairment assessed by HAQ was 0.91±0.64 [0-2.4]. Regarding the SSCI-8 score, the mean value was 17.85±6.02 [8-32]. The stigma score was not correlated with patient age (r=-0.184, p=0.075), nor with age at diagnosis (r=-0.001, p=0.993). It was not statistically different by gender (p=0.648). This score was positively correlated with DAS28 (CRP) (r=0.244, p=0.034). It was not correlated with HAQ (r=0.037, p=0.754). The presence of coxitis and the erosive nature of RA had no influence on stigma (p=0.923, p= 0.895 respectively). <h3>Conclusion</h3> According to our study, stigma was associated with disease activity during RA. The degree of stigma was not very high in our population, which can be explained by a moderately active disease. <h3>Reference</h3> [1]Molina Y, Choi SW, Cella D, Rao D. The stigma scale for chronic illnesses 8-item version (SSCI-8): development, validation and use across neurological conditions. Int J Behav Med. 2013 Sep;20(3):450-60. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.
AB0116 EVALUATING THE IMPACT OF METFORMIN TARGETS ON THE RISK OF SYSTEMIC LUPUS ERYTHEMATOSUS: A MENDELIAN RANDOMIZATION STUDY
Authors: L. L. Zheng, Y. X. Chen, C. Wang, M. J. Chang, S. X. Zhang, Q. Yu, P. F. He
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Metformin is a biguanide oral hypoglycemic agent that is widely used as a first-line drug treatment for type II diabetes. In addition, metformin is also used in the treatment of certain autoimmune diseases, such as systemic lupus erythematosus (SLE). It plays a key role in the pathogenesis of SLE through pathways such as inhibiting type 1 IFN, regulating T effector cells and proinflammatory cytokines<sup>[1]</sup>. However, the causal relationship of the metformin-related targets on the risk of SLE is still unclear. <h3>Objectives</h3> The purpose of this study was to assess the causal effect of metformin targets (AMPK, MCI, MG3, GDF 15 and GLP 1/ GCG) on the risk of SLE using Mendelian randomization (MR). <h3>Methods</h3> Genetic variants including downstream and 100 kb upstream of encoding five genes were selected as candidate tool variants. The SNP was further screened as in low linkage disequilibrium (r2 &lt; 0.3) and associated with HbA 1 c (P ≤ 0.05). The Genome-wide association study (GWAS) of HbA 1 c comes from the Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC) (n = 88,355)<sup>[2]</sup>. The SLE data (ncase = 5,201, ncontrol = 9,066) are pooled from publicly available GWAS. Two-sample MR was performed using inverse variance weighted (IVW), MR-Egger, and weighted median (WM) to obtain causal estimates of metformin-related targets and risk of SLE. In addition, sensitivity analysis, outlier (MR-PRESSO) and leave-one-out analysis were conducted to test the heterogeneity and level pleiotropy of the results. <h3>Results</h3> Genetically predicted increase in HbA1c instrumented by GDF 15 variants was associated with increased risk of SLE (GDF 15[p = 0.028]). However, genetically predicted AMPK, MG3, MCI, and GLP 1/ GCG were not associated with SLE risk (AMPK [p = 0.122], MG3 [p = 0.105], MCI [p = 0.762], GLP 1/ GCG [p = 0.361]) (Figure 1). No outlier between GDF 15 and the risk of SLE was identified via the MR-PRESSO test. The leave-one-out analysis verified the robustness of the outcomes. <h3>Conclusion</h3> This study suggests that the GDF 15 gene may be a plausible mechanism of action to reduce the risk of SLE and provides critical evidence to guide future clinical trials of metformin. <h3>References</h3> [1]Kim JW, Choe JY, Park SH. <b>Metformin and its therapeutic applications in autoimmune inflammatory rheumatic disease</b>. <i>Korean J Intern Med</i> 2022; 37(1):13-26. [2]Wheeler E, Leong A, Liu CT, Hivert MF, Strawbridge RJ, Podmore C, et al. <b>Impact of common genetic determinants of Hemoglobin A1c on type 2 diabetes risk and diagnosis in ancestrally diverse populations: A transethnic genome-wide meta-analysis</b>. <i>PLoS Med</i> 2017; 14(9):e1002383. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.